Stress can inhibit inflammatory responses critical to early wound healing by causing the release of hormones that are immunosuppressive. Thus, stress may be an important determinant in individual variance in wound healing rates. Aging has also been associated with decreased tissue responses required for wound healing, e.g., decreased metabolism, inflammatory cell infiltration and fibroblast function. Indeed, preliminary studies suggest that experimental skin wounds heal 25% slower in chronically stressed, older adults caring for Alzheimer's disease patients. The stress of taking examinations, delayed healing of oral wounds 40% as compared to non-stress conditions. In both of these studies, a key pro- inflammatory response, IL-1beta, was significantly reduced in leukocytes in stressed groups. Hypotheses: aging and psychological distress dysregulate neuroendocrine pathways, particularly glucocorticoids, that inhibit inflammatory responses critical to early wound healing. How stressors are perceived and individual differences in responsiveness to a perceived stressor can be as important as objective features of the stressor. Thus, analyses of the stressors as well as personality attributes that affect the appraisal of events as stressors and psychosocial factors, e.g., social support, that augment/buffer the perceived consequences of the stressor is essential. Furthermore, peripheral blood responses will reflect altered tissue responses during wound healing and serve as important biologic markers for stress down regulation of inflammatory cell function during wound healing. A rapidly, healing, non-scarring standardized oral wound healing model will be used to assess the affects of stress and aging in wound healing.